| pubmed-article:15718501 | rdf:type | pubmed:Citation | lld:pubmed |
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| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C0151744 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C2339371 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C0231174 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C1948027 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
| pubmed-article:15718501 | lifeskim:mentions | umls-concept:C0449774 | lld:lifeskim |
| pubmed-article:15718501 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:15718501 | pubmed:dateCreated | 2005-3-18 | lld:pubmed |
| pubmed-article:15718501 | pubmed:abstractText | Metabolic inhibition (MI) contributes to contractile failure during cardiac ischemia and systolic heart failure, in part due to decreased excitation-contraction (E-C) coupling gain. To investigate the underlying mechanism, we studied subcellular Ca2+ release patterns in whole cell patch clamped rat ventricular myocytes using two-dimensional high-speed laser scanning confocal microscopy. In cells loaded with the Ca2+ buffer EGTA (5 mmol/L) and the fluorescent Ca2+-indicator fluo-3 (1 mmol/L), depolarization from -40 to 0 mV elicited a striped pattern of Ca2+ release. This pattern represents the simultaneous activation of multiple Ca2+ release sites along transverse-tubules. During inhibition of both oxidative and glycolytic metabolism using carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP, 50 nmol/L) and 2-deoxyglucose (2-DG, 10 mmol/L), there was a decrease in inward Ca2+ current (ICa), the spatially averaged Ca2+ transient, and E-C coupling gain, but no reduction in sarcoplasmic reticulum Ca2+ content. The striped pattern of subcellular Ca2+ release became fractured, or disappeared altogether, corresponding to a marked decrease in the area of the cell exhibiting organized Ca2+ release. There was no significant change in the intensity or kinetics of local Ca2+ release. The mechanism is not fully explained by dephosphorylation of L-type Ca2+ channels, because a similar degree of ICa"rundown" in control cells did NOT result in fracturing of the Ca2+ release pattern. We conclude that metabolic inhibition interferes with E-C coupling by (1) reducing trigger Ca2+, and (2) directly inhibiting sarcoplasmic reticulum Ca2+ release site open probability. | lld:pubmed |
| pubmed-article:15718501 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15718501 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15718501 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15718501 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15718501 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15718501 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15718501 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:15718501 | pubmed:issn | 1524-4571 | lld:pubmed |
| pubmed-article:15718501 | pubmed:author | pubmed-author:GarfinkelAlan... | lld:pubmed |
| pubmed-article:15718501 | pubmed:author | pubmed-author:LampScott TST | lld:pubmed |
| pubmed-article:15718501 | pubmed:author | pubmed-author:GoldhaberJosh... | lld:pubmed |
| pubmed-article:15718501 | pubmed:author | pubmed-author:BridgeJohn... | lld:pubmed |
| pubmed-article:15718501 | pubmed:author | pubmed-author:MotterChristi... | lld:pubmed |
| pubmed-article:15718501 | pubmed:author | pubmed-author:FukumotoGary... | lld:pubmed |
| pubmed-article:15718501 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:15718501 | pubmed:day | 18 | lld:pubmed |
| pubmed-article:15718501 | pubmed:volume | 96 | lld:pubmed |
| pubmed-article:15718501 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15718501 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15718501 | pubmed:pagination | 551-7 | lld:pubmed |
| pubmed-article:15718501 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:15718501 | pubmed:meshHeading | pubmed-meshheading:15718501... | lld:pubmed |
| pubmed-article:15718501 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15718501 | pubmed:articleTitle | Metabolic inhibition alters subcellular calcium release patterns in rat ventricular myocytes: implications for defective excitation-contraction coupling during cardiac ischemia and failure. | lld:pubmed |
| pubmed-article:15718501 | pubmed:affiliation | Department of Medicine, Cardiovascular Research Laboratories, Geffen School of Medicine at UCLA, Los Angeles, Calif 90095-1679, USA. | lld:pubmed |
| pubmed-article:15718501 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15718501 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15718501 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:15718501 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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